✦ LIBER ✦

Decrease of TGF-β1 plasma levels and increase of nitric oxide synthase activity in leukocytes as potential biomarkers of Alzheimer's disease

✍ Scribed by B. De Servi; C.A.M. La Porta; M. Bontempelli; R. Comolli

Book ID: 114253727
Publisher: Elsevier Science
Year: 2002
Tongue: English
Weight: 154 KB
Volume: 37
Category: Article
ISSN: 0531-5565
DOI: 10.1016/s0531-5565(02)00018-9

No coin nor oath required. For personal study only.

📜 SIMILAR VOLUMES

Increased plasma levels of soluble CD40,

Increased plasma levels of soluble CD40, together with the decrease of TGFβ1, as possible differential markers of Alzheimer disease

✍ A. Mocali; S. Cedrola; N. Della Malva; M. Bontempelli; V.A.M. Mitidieri; A. Bava 📂 Article 📅 2004 🏛 Elsevier Science 🌐 English ⚖ 173 KB

Characterization of plasma β-secretase (

Characterization of plasma β-secretase (BACE1) activity and soluble amyloid precursor proteins as potential biomarkers for Alzheimer's disease

✍ Guoxin Wu; Sethu Sankaranarayanan; Jacky Wong; Katherine Tugusheva; Maria S. Mic 📂 Article 📅 2012 🏛 John Wiley and Sons 🌐 English ⚖ 814 KB

Increased concentrations of homocysteine

Increased concentrations of homocysteine and asymmetric dimethylarginine and decreased concentrations of nitric oxide in the plasma of patients with Alzheimer’s disease

✍ M.L. Selley 📂 Article 📅 2003 🏛 Elsevier Science 🌐 English ⚖ 76 KB

Decreased levels of PSD95 and two associ

Decreased levels of PSD95 and two associated proteins and increased levels of BCl2 and caspase 3 in hippocampus from subjects with amnestic mild cognitive impairment: Insights into their potential roles for loss of synapses and memory, accumulation of Aβ, and neurodegeneration in a prodromal stage of Alzheimer's disease

✍ Rukhsana Sultana; William A. Banks; D. Allan Butterfield 📂 Article 📅 2009 🏛 John Wiley and Sons 🌐 English ⚖ 218 KB

## Abstract Alzheimer's disease (AD) is the most common form of dementia and is pathologically characterized by senile plaques, neurofibrillary tangles, synaptic disruption and loss, and progressive neuronal deficits. The exact mechanism(s) of AD pathogenesis largely remain unknown. With advances i